How a Brain Injury Tells The Body it is Hurt

 

Brain Injury – Johns Hopkins researchers say they have identified a new way that cells in the brain alert the rest of the body to recruit immune cells when the brain is injured. The work was completed in mouse models that mimic infection, stroke or trauma in humans.

 

Investigators already knew there was a communication highway between the brain and the immune system but have been unclear about how exactly how the brain sends signals to the immune system. While immune system cells’ purpose is to defend and protect the body, ironically the brain’s “call to arms” may cause more harm than good when it instructs immune cells to enter into the brain. The persistence of these cells can cause chronic inflammation and damage the brain.

In their new study, described in Science Signaling April 13, Johns Hopkins researchers say there is evidence that vesicles or small (about the size of a virus), fat-like molecules and protein-filled sacks released from a type of immune cell in the brain called astrocytes travel through the bloodstream to the liver. The liver then instructs white blood cells to go to the site of injury in the brain.

“This work describes an entirely new way that the brain talks with the body,” says Norman Haughey, Ph.D., professor of neurology at the Johns Hopkins University School of Medicine. “Identifying this pathway has helped us pinpoint ways to impede this process and reduce brain damage brought on by the body’s own excessive immune response.”

Because of the work of several other collaborators, Haughey says, his team knew that some sort of inflammation-promoting molecule was released from brain and targeted to the liver after brain injury to send immune system cells to the damaged area, but the identity of this go-between had been elusive for years.

The questions remained of what the signal was, and how, exactly, the signal got all the way to the liver from the brain, particularly since the blood-brain barrier prevents many molecules in the brain from crossing over into the rest of the body, just as it prevents molecules from getting into the brain. The team focused on an enzyme called neutral sphingomyelinase, known as nSMase2, which they knew from a separate project was turned on by an immune system chemical messenger, a cytokine interleukin 1-beta (IL-1b) that promotes inflammation. Sphingomyelinases like nSMase2 play a normal role in the cell’s metabolism by breaking down fatty molecules into smaller components that cells use for every day functions.

To see if possibly nSMase2 was also involved in alerting the immune system during brain injury, the researchers mimicked brain injury in mice by injecting cytokine IL-1b into the striatum, a structure found in the deep center of the brain. As a comparison group, they injected saline (saltwater) in the same brain area of other mice. They also injected the mouse brains with both the cytokine IL-1b and a drug called altenusin that blocks the nSMase enzyme from working.

Twenty-four hours after the injection, the researchers saw large numbers of immune system white blood cells in tissue samples of the rodent brains near the site of injury of those mice injected with the cytokine IL-1b, but not in the brain tissue of the control group of mice. In addition, they no longer saw the same large influx of white blood cells into the brain when they used the drug that inhibited nSMase, with the number of white blood cells in the brain dropping by about 90 percent. This finding told the researchers of nSMase2’s involvement but still didn’t tell them about the signal sent from the brain to activate the body’s immune response. According to Haughey, after many failed experiments to determine the brain’s messenger, he visited his colleague and collaborator Daniel Anthony at Oxford University, who introduced him to the concept of “exosomes” — miniature vesicles released from cells.

“That conversation was the ‘Ah-ha’ moment when it all began to make sense,” says Haughey.

He read earlier studies showing that the enzyme nSMase2 was required for forming and releasing exosomes. Exosomes form inside cell compartments and release outside the cell when these compartments fuse with the cell’s surrounding membrane. Exosomes are surrounded by bits of cell membrane and filled with proteins and different types of the genetic material RNA.

To test that exosomes were the source of this brain to body communication, Haughey’s research team isolated exosomes from the blood of mice four hours after injecting the cytokine IL-1b into brain and then injected the exosomes into the tail veins of different mice that had the cytokine and the nSMase-blocking drug altenusin already in their brains.

The researchers found that white blood cells in healthy mice who received exosomes from the blood of the mice with brain damage traveled to the site of brain injury, which the researchers say demonstrates that exosomes released from brain in response to damage alert the immune system to send the immune cell sentinels to the brain.

When they stripped the vesicles of protein and their genetic cargo and injected them back into mice, the blood cells no longer went to the site of brain injury.

Finally, the researchers analyzed the protein and genetic material contents of the exosomes in an effort to identify the molecules inside that alerted the immune system to brain damage. They found 10 unique proteins and 23 microRNAs — short bits of RNA that don’t code for genes — at increased levels in the vesicles. Several of these components had connections to a specific mechanism used by the liver to activate inflammation.

“Given the therapeutic potential of the nSMase target, we’re now working closely with Drs. Barbara Slusher, Camilo Rojas, Ajit Thomas and colleagues at the Johns Hopkins Drug Discovery facility to identify potent inhibitors of the nSMase enzyme which can be developed for clinical use,” says Haughey.


 

Story Source:

Materials provided by Johns Hopkins Medicine. Note: Content may be edited for style and length.


 

Journal Reference:

Alex M. Dickens, Luis B. Tovar-y-Romo, Seung-Wan Yoo, Amanda L. Trout, Mihyun Bae, Marlene Kanmogne, Bezawit Megra, Dionna W. Williams, Kennith W. Witwer, Mar Gacias, Nino Tabatadze, Robert N. Cole, Patrizia Casaccia, Joan W. Berman, Daniel C. Anthony, Norman J. Haughey. Astrocyte-shed extracellular vesicles regulate the peripheral leukocyte response to inflammatory brain lesions. Science Signaling, 2017; 10 (473): eaai7696 DOI:10.1126/scisignal.aai7696

 

Citation:

Johns Hopkins Medicine. “How the injured brain tells the body it’s hurt.” ScienceDaily. ScienceDaily, 18 May 2017. <www.sciencedaily.com/releases/2017/05/170518104041.htm>.

Sleep is Important in the Healing of TBI

There is a link between the amount of sleep the patient gets and the rate at which their brain heals.

A study of 30 people that were hospitalized for moderate to severe traumatic brain injuries found that sleep quality and brain function improved in tandem, researchers reported in the journal Neurology.

“Patients who still had low levels of consciousness and cognitive functioning would “sleep for a couple of minutes and then wake up for a couple of minutes,” both day and night, says Nadia Gosselin.

The results increase the possibility that patients with brain injuries possibly recover even quicker if hospitals would take measures  to restore normal sleep patterns, Gosselin says. Drugs are one option, she says. Another is making sure patients are exposed to sunlight or its equivalent during the day and at night rest in a dark, quiet environment.

“I think bad sleep can have bad consequences for brain recovery,” she concludes.

New Test to Quickly Identify Mild Traumatic Brain Injury

A new test using peripheral vision reaction time could lead to earlier diagnosis and more effective treatment of mild traumatic brain injury, often referred to as a concussion. Identify Brain Injury

A new test using peripheral vision reaction time could lead to earlier diagnosis and more effective treatment of mild traumatic brain injury, often referred to as a concussion, according to Peter J. Bergold, PhD, professor of physiology and pharmacology at SUNY Downstate Medical Center and corresponding author of a study newly published online by the Journal of Neurotrauma.

While most patients with mild traumatic brain injury or concussion fully recover, a significant number do not, and earlier diagnosis could lead to better management of patients at risk for developing persistent symptoms, according to Dr. Bergold and his co-authors.

Lingering symptoms may include loss of concentration and/or memory, confusion, anxiety, headaches, irritability, noise and light sensitivity, dizziness, and fatigue.

“Mild traumatic brain injury is currently diagnosed with subjective clinical assessments,” says Dr. Bergold. “The potential utility of the peripheral vision reaction test is clear because it is an objective, inexpensive, and rapid test that identifies mild traumatic brain injury patients who have a more severe underlying injury.”

Dr. Bergold’s co-authors include colleagues from the University of Texas Southwestern Medical Center; The University of Texas at Dallas; Washington University; the National Institute of Neurological Disorders and Stroke; the Uniformed Services University of the Health Sciences; and SUNY Downstate.

The article published by the Journal of Neurotrauma is titled “Measurement of Peripheral Vision Reaction Time Identifies White Matter Disruption in Patients with Mild Traumatic Brain Injury.”

[embedyt] http://www.youtube.com/watch?v=aKZnMC5vzhU[/embedyt]


Story Source:

Materials provided by SUNY Downstate Medical Center. Note: Content may be edited for style and length.


Journal Reference:

  1. Kyle B. Womack, Christopher Paliotta, Jeremy F. Strain, Johnson S. Ho, Yosef Skolnick, William W. Lytton, L. Christine Turtzo, Roderick McColl, Ramon Diaz-Arrastia, Peter J. Bergold. Measurement of Peripheral Vision Reaction Time Identifies White Matter Disruption in Patients with Mild Traumatic Brain Injury. Journal of Neurotrauma, 2017; DOI:10.1089/neu.2016.4670

SUNY Downstate Medical Center. “New test may quickly identify mild traumatic brain injury with underlying brain damage.” ScienceDaily. ScienceDaily, 16 February 2017. <www.sciencedaily.com/releases/2017/02/170216120538.htm>.

 

What is a Diffuse Axonal Injury? (DAI)

As tissue slides over tissue, a shearing injury occurs. This causes the lesions that are responsible for unconsciousness, as well as the vegetative state that occurs after a severe head injury. A diffuse axonal injury also causes brain cells to die, which cause swelling in the brain.”
DAI is characterized by axonal separation, in which the axon is torn at the site of stretch and the part distal to the tear degrades. While it was once thought that the main cause of axonal separation was tearing due to mechanical forces during the trauma, it is now understood that axons are not typically torn upon impact; rather, secondary biochemical cascades, which occur in response to the primary injury (which occurs as the result of mechanical forces at the moment of trauma) and take place hours to days after the initial injury, are largely responsible for the damage to axons.
Though the processes involved in secondary brain injury are still poorly understood, it is now accepted that stretching of axons during injury causes physical disruption to and proteolytic degradation of the cytoskeleton.[1] It also opens sodium channels in the axolemma, which causes voltage-gated calcium channels to open and Ca2+ to flow into the cell. The intracellular presence of Ca2+ unleashes several different pathways, including activating phospholipases and proteolytic enzymes, damaging mitochondria and the cytoskeleton, and activating secondary messengers, which can lead to separation of the axon and death of the cell.

Tips on How To Recover from a TBI

Recovering from a Brain Injury could be a long and grueling process, especially if you do not have the information to better assist you to heal.  In this post, we go over how to help accelerate the healing of your brain.

Recover – Get a lot of rest around evening time, and rest amid the day.
Maintain a strategic distance from exercises that are physically requesting (e.g., substantial housecleaning, weightlifting/working-out) or require a considerable measure of fixation (e.g., adjusting your checkbook). They can exacerbate your manifestations and moderate your recuperation.

Stay away from exercises, for example, contact or recreational games, that could prompt to another blackout (it is best to maintain a strategic distance from fast entertainment mecca rides that can exacerbate your side effects or even cause a blackout).
At the point when your medicinal services proficient says you are alright, come back to your typical exercises bit by bit, not at the same time.
Since your capacity to respond might be slower after a blackout, ask your social insurance proficient when you can securely drive an auto, ride a bicycle, or work overwhelming gear.
Converse with your medicinal services proficient about when you can come back to work. Get some information about how you can help your boss comprehend what has transpired.
Consider chatting with your boss about coming back to work step by step and about changing your work exercises or timetable until you recoup (e.g., work half-days).
Take just those medications that your medicinal services proficient has endorsed.
Try not to drink mixed refreshments until your social insurance proficient says you are all around ok. Liquor and different medications may moderate your recuperation and put you at danger of further damage.
Record the things that might be harder than regular for you to recollect.
In case you’re effectively occupied, attempt to do one thing at any given moment. For instance, don’t attempt to sit in front of the TV while settling supper.
Counsel with relatives or dear companions when settling on essential choices.
Try not to disregard your fundamental needs, for example, eating great and getting enough rest.
Maintain a strategic distance from supported PC utilize, including PC/computer games ahead of schedule in the recuperation procedure.
A few people report that flying in planes aggravates their side effects soon after a blackout.

Positive Thoughts, Positive Results

Audio:

“Through my own experience dealing with a TBI, I found it beneficial to think positive, not only to me; but the world around me.” -Ryan

There may be no different choice around it, sorry…
you will enjoy negativity in your lifestyles–maybe on a day by day incidence.
There may be some of those days in which you want you stayed inside, laid on the mattress and played tag with the snooze button. There can be those days in which the people, locations, matters and events in your existence come collectively to shape one massive large mass of ‘suck’. As they are saying, things happen. For us in the ‘healing process’, the technique of navigating the bad that takes place to us can be an thrilling experience.
I am now not saying that the mere sliver of negativity will compel you to hurry without delay to the liquor store, corner tavern or your supplier, but in case you let the terrible things simmer and stew inside the crockpot of the soul chances are going to be almost exact that we are able to smell what we are cookin’ and it’ll not indicate properly for us.
The negative events that we encounter in our day-to-day doings are one of the most not unusual snares that we can fall into in regards to relapse. It’s sincerely crucial to stand what stresses, angers, and frustrates us head-on, but ‘cooking’ inside the juices of adversity and permitting it to run insurrection is ‘no bueno‘. How can we maintain the finger off the cause at the same time as shifting forward and keeping our sanity intact?
Understand the power of superb wondering in healing.
We ‘suppose’ a lot
have you ever ever thought approximately how many thoughts you’ve got in a single day?
Consistent with some estimates, we as people average between 40,000 to 60,000 different thoughts an afternoon. Isn’t that remarkable??  That may be a ton of information that passes thru our gray rely, and it’s miles a secure bet that a honest percent of those mind are the ones that motive us grief and problem to various tiers. Paying payments, elevated workload or college work, family issues, tickets, remembering to take the kids to soccer practice/dance class/lacrosse…the listing can go on and on…
It’s no wonder why there are days when we lay down and experience like we have been hit with the aid of a truck. Bad electricity drains us and breaks us down, and if we permit ourselves to stay stuck within the doom and gloom the manner we view ourselves, others and the world round us starts to bitter. While we live in Debbie Downer mode, we are extra prone to feeling prolonged periods of depression and anxiety because we stay caught in emotions of anger, frustration and hopelessness–and that is horrific in we’re looking to maintain our sobriety.
While we stay stuck in negativity, we’re at greater danger for growing high blood pressure, elevated times of infections, cardiovascular ailment and digestive problems. Moreover, research has shown that continual pressure and negativity can genuinely lower our lifespan with the aid of shortening our telomeres (the “end caps” of our DNA strands, which play a massive role in getting older).
It’s miles truly essential that we include advantageous wondering in recuperation if you want to stay on the level. As with the whole lot that we do in recuperation, staying wonderful in sobriety takes realize how.
Embracing Positivity In recovery
whilst you are careworn with the grind of existence and are weighed down via the negative, you’ll be amazed to analyze that some of the things that we agonize and dread in reality flip out for the pleasant. How many instances has that happened to you?  Our pals at Happify daily proportion the following:
85 percent of the stuff we fear about end up having a tremendous or neutral final results.
Inside the occasion that what we fear about becomes reality, eighty percent of humans say they treated the outcome higher than they thought they could.
In our recuperation, it is important to maintain this in mind. We regularly pay attention around the tables of 12-step meetings the phrase this too shall pass, and at the same time as this pronouncing is properly-worn (and dare we say cliche) it’s miles absolutely the fact. Whether or not we believe it or no longer, we have an enormous power in reserve and we can persevere and pull via matters regardless of what the chances.
Easy recommendations to growth Positivity in your recovery
when we talk of positivity in recuperation, you already possess a number of the tools you want. When you have are in a drug remedy application or have already efficiently finished a treatment program, you had been taught the simple but essential life skills needed to keep your recuperation game on point at the same time as efficaciously navigating the molehills and mountains of daily existence.
You can additionally have picked up some of those abilities on your homegroup, via operating along with your sponsor or through a member of the family or pal. The subsequent are easy ways that you may incorporate and enhance tremendous questioning for your healing.
Meditate
One manner to increase your tremendous questioning in recuperation is through the usage of meditation. Meditation is a powerful device which you have at your disposal, and if you may carve out 15 mins an afternoon you may advantage first-rate advantage. Whether it is simple aware meditation practices or greater formal meditation practices, focusing on your breathing is enjoyable and allows you attention on the here and now and the way you can impact the present. Whilst you exercise meditation frequently, any mind of the past or future fall to the sides and you can place your energies on what you may do right now to be happier.
Take duty in your existence
you know this, but you on my own are liable for your life, and also you on my own have the power to convert your life. This simple truth can be difficult to border in our minds due to the fact we often pinned the blame on others when we had been lively in our dependancy. As stated in advance, we’ve limitless electricity that resides inside us and while the chips are down we may be amazed at how we are able to pull through. Now could be the time to position the capabilities and realize how to proper use.
Stick with the Winners
if you need to come to be greater nice, you want fantastic role models. Another one of the commonplace announcing heard in 12-Step meetings is stay with the winners and the that means is simple. You want to dangle with folks that meet adversity of their existence with energy and fortitude. Whether or not is it your peers in restoration, circle of relatives participants, friends or whomever, discover the ones people in your lifestyles who recognise how to deal with negativity in a wholesome, constructive and sensible way and soak their know-how in like a sponge.
Be of provider to a person
in order to tug out of a tailspin, it is good to get out of your self and be of carrier to someone else. Volunteer your time at a drop-in middle, senior citizen home, or nearby sanatorium. Be a mentor or a sponsor to someone who’s new in recovery.
Smile
To generate positive mind for your healing, every now and then you simply ought to faux it that allows you to make it. You can not sense like it or up to it, however the easy act of placing a grin in your face may additionally help you get out of the doldrums. It’s miles often said that it takes extra muscle tissue and strength to frown than it’s far to grin. Simply the simple act of a grin could make you feel lighter. Provide it a attempt.

 

Diffuse Axonal Injury

Audio:

Diffuse Axonal Injury (DAI) A  brain injury, in which damage is in the form of extensive lesions in white matter tracts occurs over a widespread area. DAI is one of the most prevalent and devastating types of traumatic brain injury, DAIs are a major cause of unconsciousness and most likely, leads to vegetative state after severe head trauma. The outcome is frequently a coma, with over 90% of patients with severe DAI never again, regaining consciousness. Those who do wake up often remain significantly impaired.

DAI can occur in every measure of severity from very mild or moderate to very severe

 

Diffuse axonal injury (DAI) is a brain injury in which damage in the form of extensive lesions in white matter tracts occurs over a widespread area. DAI is one of the most common and devastating types of traumatic brain injury,[1] and is a major cause of unconsciousness and persistent vegetative state after severe head trauma.[2] It occurs in about half of all cases of severe head trauma and may be the primary damage that occurs in concussion. The outcome is frequently coma, with over 90% of patients with severe DAI never regaining consciousness. Those who do wake up often remain significantly impaired.

 

  • DAI can occur in every degree of severity from very mild or moderate to very severe. Concussion may be a milder type of diffuse axonal injury.
  • Mechanism
  • Unlike brain trauma that occurs due to direct impact and deformation of the brain, DAI is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated, as may occur in car accidents, falls, and assaults.[5] It usually results from rotational forces or severe deceleration. Vehicle accidents are the most frequent cause of DAI; it can also occur as the result of child abuse[6] such as in shaken baby syndrome.
  • The major cause of damage in DAI is the disruption of axons, the neural processes that allow one neuron to communicate with another. Tracts of axons, which appear white due to myelination, are referred to as white matter. Acceleration causes shearing injury: damage inflicted as tissue slides over other tissue. When the brain is accelerated, parts of differing densities and distances from the axis of rotation slide over each other, stretching axons that traverse junctions between areas of different density, especially at junctions between white and grey matter. Two-thirds of DAI lesions occur in areas where grey and white matter meet.
  • Characteristics
  • Lesions typically exist in the white matter of brains injured by DAI; these lesions vary in size from about 1–15 mm and are distributed in a characteristic way. DAI most commonly affects white matter in areas including the brain stem, the corpus callosum, and the cerebral hemispheres.
  • The lobes of the brain most likely to be injured are the frontal and temporal lobes. Other common locations for DAI include the white matter in the cerebral cortex, the superior cerebral peduncles, basal ganglia, thalamus, and deep hemispheric nuclei. These areas may be more easily damaged because of the difference in density between them and the rest of the brain.
  • Histological characteristics
  • DAI is characterized by axonal separation, in which the axon is torn at the site of stretch and the part distal to the tear degrades. While it was once thought that the main cause of axonal separation was tearing due to mechanical forces during the trauma, it is now understood that axons are not typically torn upon impact; rather, secondary biochemical cascades, which occur in response to the primary injury (which occurs as the result of mechanical forces at the moment of trauma) and take place hours to days after the initial injury, are largely responsible for the damage to axons.
  • Though the processes involved in secondary brain injury are still poorly understood, it is now accepted that stretching of axons during injury causes physical disruption to and proteolytic degradation of the cytoskeleton.[1] It also opens sodium channels in the axolemma, which causes voltage-gated calcium channels to open and Ca2+ to flow into the cell.[1] The intracellular presence of Ca2+ unleashes several different pathways, including activating phospholipases and proteolytic enzymes, damaging mitochondria and the cytoskeleton, and activating secondary messengers, which can lead to separation of the axon and death of the cell.
  • Cytoskeleton disruption-
  • Immunoreactive axonal profiles are observed as either granular (B,G,H) or more elongated, fusiform (F) swellings in the corpus callosum and the brain stem (H) at 24h post traumatic brain injury. Example of APP-immunoreactive neurons (arrow heads) observed in the cortex underneath the impact site (E,G). No APP staining was observed in healthy control animals (D).
  • Axons are normally elastic, but when rapidly stretched they become brittle, and the axonal cytoskeleton can be broken. Misalignment of cytoskeletal elements after stretch injury can lead to tearing of the axon and death of the neuron. Axonal transport continues up to the point of the break in the cytoskeleton, but no further, leading to a buildup of transport products and local swelling at that point. When it becomes large enough, swelling can tear the axon at the site of the break in the cytoskeleton, causing it to draw back toward the cell body and form a bulb. This bulb is called a retraction ball, the hallmark of diffuse axonal injury.
  • When the axon is transected, Wallerian degeneration, in which the part of the axon distal to the break degrades, takes place within one to two days after injury. The axolemma disintegrates, myelin breaks down and begins to detach from cells in an anterograde direction (from the body of the cell toward the end of the axon),and nearby cells begin phagocytic activity, engulfing debris.
  • Calcium influx
  • While sometimes only the cytoskeleton is disturbed, frequently disruption of the axolemma occurs as well, causing the influx of Ca2+ into the cell and unleashing a variety of degrading processes. An increase in Ca2+ and Na+ levels and a drop in K+ levels is found within the axon directly after injury. Possible routes of Ca2+ entry include sodium channels, pores torn in the membrane during stretch, and failure of ATP-dependent transporters due to mechanical blockage or lack of energy. High levels of intracellular Ca2+, the major cause of post-injury cell damage, destroy mitochondria,and trigger phospholipases and proteolytic enzymes that damage Na+ channels and degrade or alter the cytoskeleton and the axoplasm. Excess Ca2+ can also lead to damage to the blood brain barrier and swelling of the brain.
  • One of the proteins activated by the presence of calcium in the cell is calpain, a Ca2+-dependent non-lysosomal protease. About 15 minutes to half an hour after the onset of injury, a process called calpain-mediated spectrin proteolysis, or CMSP, begins to occur.[19] Calpain breaks down a molecule called spectrin, which holds the membrane onto the cytoskeleton, causing the formation of blebs and the breakdown of the cytoskeleton and the membrane, and ultimately the death of the cell.[18][19] Other molecules that can be degraded by calpains are microtubule subunits, microtubule-associated proteins, and neurofilaments.
  • Generally occurring one to six hours into the process of post-stretch injury, the presence of calcium in the cell initiates the caspase cascade, a process in cell injury that usually leads to apoptosis, or “cell suicide”.
  • Mitochondria, dendrites, and parts of the cytoskeleton damaged in the injury have a limited ability to heal and regenerate, a process which occurs over 2 or more weeks. After the injury, astrocytes can shrink, causing parts of the brain to atrophy.
  • Diagnosis
  • Diffuse axonal injury after a motorcycle accident. MRI after 3 days: on T1-weighted images the injury is barely visible. On the FLAIR, DWI and T2* weighted images a small bleed is appreciated.
  • DAI is difficult to detect since it does not show up well on CT scans or with other macroscopic imaging techniques, though it shows up microscopically. However, there are characteristics typical of DAI that may or may not show up on a CT scan. Diffuse injury has more microscopic injury than macroscopic injury and is difficult to detect with CT and MRI, but its presence can be inferred when small bleeds are visible in the corpus callosum or the cerebral cortex. MRI is more useful than CT for detecting characteristics of diffuse axonal injury in the subacute and chronic time frames. Newer studies such as Diffusion Tensor Imaging are able to demonstrate the degree of white matter fiber tract injury even when the standard MRI is negative. Since axonal damage in DAI is largely a result of secondary biochemical cascades, it has a delayed onset, so a person with DAI who initially appears well may deteriorate later. Thus injury is frequently more severe than is realized, and medical professionals should suspect DAI in any patients whose CT scans appear normal but who have symptoms like unconsciousness.
  • MRI is more sensitive than CT scans, but MRI may also miss DAI, because it identifies the injury using signs of edema, which may not be present.
  • DAI is classified into grades based on severity of the injury. In Grade I, widespread axonal damage is present but no focal abnormalities are seen. In Grade II, damage found in Grade I is present in addition to focal abnormalities, especially in the corpus callosum. Grade III damage encompasses both Grades I and II plus rostral brain stem injury and often tears in the tissue.[23]
  • Treatment
  • DAI currently lacks a specific treatment beyond what is done for any type of head injury, including stabilizing the patient and trying to limit increases in intracranial pressure (ICP).
  • History
  • The idea of DAI first came about as a result of studies by Sabina Strich on lesions of the white matter of individuals who had suffered head trauma years before.[24] Strich first proposed the idea in 1956, calling it diffuse degeneration of white matter, however, the more concise term “Diffuse Axonal Injury” was eventually preferred. Strich was researching the relationship between dementia and head trauma and asserted in 1956 that DAI played an integral role in the eventual development of dementia due to head trauma. The term DAI was introduced in the early 1980s.

TBI Recovery Phases, Short/Long-Term Impacts

Audio:

Like almost everything else in life, recovering from a TBI is a process. This article will make you aware of the different stages of that process.

—————

Common stages

In the first few weeks after a brain injury, swelling, bleeding or changes in brain chemistry often affect the function of healthy brain tissue. The injured person’s eyes may remain closed, and the person may not show signs of awareness. As swelling decreases and blood flow and brain chemistry improve, brain function usually improves. With time, the person’s eyes may open, sleep-wake cycles may begin, and the injured person may follow commands, respond to family members, and speak. Some terms that might be used in these early stages of recovery are:

  • Coma: The person is unconscious, does not respond to visual stimulation or sounds, and is unable to communicate or show emotional responses.
  • Vegetative State: The person has sleep-wake cycles, and startles or briefly orients to visual stimulation and sounds.
  • Minimally Conscious State: The person is partially conscious, knows where sounds and visual stimulation are coming from, reaches for objects, responds to commands now and then, can vocalize at times, and shows emotion.

A period of confusion and disorientation often follows a TBI. A person’s ability to pay attention, agitation, nervousness, restlessness or frustration may appear. Sleeping patterns may be disrupted. The person may overreact to stimulation and become physically aggressive. This stage can be disturbing for family because the person behaves so uncharacteristically.

Inconsistent behavior is also common. Some days are better than others. For example, a person may begin to follow a command (lift your leg, squeeze my finger) and then not do so again for a time. This stage of recovery may last days or even weeks for some. In this stage of recovery, try not to become anxious about inconsistent signs of progress. Ups and downs are normal.

Later stages of recovery can bring increased brain and physical function. The person’s ability to respond may improve gradually.

Length of Recovery:

The fastest improvement happens in about the first six months after injury. During this time, the injured person will likely show many improvements and may seem to be steadily getting better. The person continues to improve between six months and two years after injury, but this varies for different people and may not happen as fast as the first six months. Improvements slow down substantially after two years but may still occur many years after injury. Most people continue to have some problems, although they may not be as bad as they were early after injury. Rate of improvement varies from person to person.

Long-term impacts:

It is common and understandable for family members to have many questions about the long-term effects of the brain injury on the injured person’s ability to function in the future. Unfortunately, it is difficult to determine the long-term effects for many reasons.

  • First, brain injury is a relatively new area of treatment and research. We have only begun to understand the long-term effects in patients one, five, and ten years after injury.
  • Brain scans and other tests are not always able to show the extent of the injury, so it is sometimes difficult early on to fully understand how serious the injury is.
  • The type of brain injury and extent of secondary problems such as brain swelling varies a great deal from person to person.
  • Age and pre-injury abilities also affect how well a person will recover.

We do know that the more severe the injury the less likely the person will fully recover. The length of time a person remains in a coma and duration of loss of memory (amnesia) following the coma are useful in predicting how well a person will recover.

The Rancho Los Amigos Levels of Cognitive Functioning (RLCF) is one of the best and most widely used ways of describing recovery from brain injury. The RLCF describes ten levels of cognitive (thinking) recovery. Research has shown that the speed at which a person progresses through the levels of the RLCF can predict how fully a person will recover.

The Rancho Los Amigos Levels of Cognitive Functioning:

Level 1– No Response: Person appears to be in a deep sleep.

Level 2– Generalized Response: Person reacts inconsistently and not directly in response to stimuli.

Level 3– Localized Response: Person reacts inconsistently and directly to stimuli.

Level 4– Confused/Agitated: Person is extremely agitated and confused.

Level 5– Confused-Inappropriate/Non-agitated: Person is confused and responses to commands are inaccurate.

Level 6– Confused-Appropriate: Person is confused and responds accurately to commands.

Level 7– Automatic-Appropriate: Person can go through daily routine with minimal to no confusion.

Level 8– Purposeful-Appropriate: Person has functioning memory, and is aware of and responsive to their environment.

Level 9– Purposeful-Appropriate: Person can go through daily routine while aware of need for stand by assistance.

Level 10– Purposeful-Appropriate/Modified Independent: Person can go through daily routine but may require more time or compensatory strategies.

 

Recovery two years after brain injury

Based on information of people with moderate to severe TBI who received acute medical care and inpatient rehabilitation services at a TBI Model System, two years post-injury:

  • Most people continue to show decreases in disability.
  • 34% of people required some level of supervision during the day and/or night.
  • 93% of people are living in a private residence.
  • 34% are living with their spouse or significant other; 29% are living with their parents.
  • 33% are employed; 29% are unemployed; 26% are retired due to any reason; and 3% are students.

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Disclaimer

This information is not meant to replace the advice from a medical professional. You should consult your health care provider regarding specific medical concerns or treatment.

Source

Our health information content is based on research evidence whenever available and represents the consensus of expert opinion of the TBI Model Systems directors.

Our health information content is based on research evidence and/or professional consensus and has been reviewed and approved by an editorial team of experts from the TBI Model Systems.

Authorship

Understanding TBI was developed by Thomas Novack, PhD and Tamara Bushnik, PhD in collaboration with the Model System Knowledge Translation Center. Portions of this document were adapted from materials developed by the Mayo Clinic TBIMS, Baylor Institute for Rehabilitation, and from Picking up the pieces after TBI: A guide for Family Members, by Angelle M. Sander, PhD, Baylor College of Medicine (2002).

Understanding TBI: Part 3 – The Recovery Process. (n.d.). Retrieved February 14, 2017, from http://www.msktc.org/tbi/factsheets/Understanding-TBI/The-Recovery-Process-For-Traumatic-Brain-Injury

‘Effects of a TBI’

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Intellectual impacts can include:

Here and now memory misfortune and/or long haul memory misfortune

Eased back capacity to process data, particularly recently procured data

Inconvenience focusing or focusing for timeframes

Trouble staying aware of a discussion; other correspondence challenges, for example, word discovering issues

Spatial confusion

Debilitated judgment

Not able to accomplish more than one thing at any given moment

A failure to start exercises, or once began, trouble in finishing assignments without updates

Physical handicaps are normal, yet not generally present. A few illustrations are loss of motion, loss of coordination, discourse issues, and also disability of vision, hearing and different faculties.

Passionate issues can include:

Expanded uneasiness

Discouragement and emotional episodes

Incautious conduct

All the more effortlessly disturbed

Egocentric practices; trouble perceiving how one’s own particular practices can influence others

Survivors of mind harm require professional, recreational, and private administrations so as to understand any advance in adapting, living with their cerebrum damage, and assembling their lives back.

 

Traumatic Brain Injury Facts. (n.d.). Retrieved February 14, 2017, from http://www.bcftbi.org/about-tbi/facts.asp

Myths & Facts About TBI

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There are numerous basic confusions or myths about cerebrum wounds among kids. Some of these myths were accepted to be valid before. Others are ‘clinical legend’ that has been passed starting with one educator, clinician or doctor then onto the next.

 

Myth 1: When an understudy looks great, they are completely recuperated.

Reality: The better an understudy looks, the harder it is to perceive their learning and intellectual needs. This is basic on the grounds that physical recuperation commonly precedes intellectual recuperation and occurs at a quicker rate. Frequently understudies are misidentified as having consideration or learning issues after their physical wounds have mended.

Myth 2: A mellow mind harm (blackout) is gentle and less harming than other cerebrum wounds.

Certainty: Although around 90% of individuals who have blackouts recuperate, this is not the situation for everybody. Blackout, whiplash and other “gentle” cerebrum wounds can have durable, incapacitating impacts that need intercession.

Myth 3: Younger people mend better – a youthful mind can recuperate itself, or the part that may have been harmed isn’t created yet.

Certainty: A more youthful mind is more powerless against harm in light of the fact that undeveloped parts develop from the beforehand harmed territories; this makes future improvement hard to foresee.

Myth 4: An understudy who tests in the ordinary range can learn new material well.

Truth: Evaluations regularly test already learned data, not how an understudy adapts new data. A superior expectation of an understudy’s capacity to learn new data is to educate new data and after that test for comprehension. Additionally consider the understudy’s capacity to screen out clamor and movement, which are constants in many classrooms.

Myth 5: Recovery will take ‘about’ a year.

Certainty: When a tyke has a cerebrum damage, the idea of recuperation might deceive. Recuperation ordinarily implies somebody has lost capacities briefly and will recapture them, for example, a broken arm. For a man with a cerebrum damage, despite the fact that they may look the same the progressions are in all likelihood durable and modification is a continuous procedure.

Myth 6: How rapidly a tyke recoups from a cerebrum damage depends predominantly on how hard they function at recuperating.

Actuality: No two youngsters with cerebrum wounds are indistinguishable and recuperation shifts broadly between kids with comparable wounds. It is uncalled for to an understudy to gain expectations or judgments about their ground.

Myth 7: If the cerebrum damage were truly extraordinary, the understudy would have been in the clinic for quite a while.

Certainty: Some youngsters with genuine mind wounds don’t have similar options accessible to them that grown-ups accomplish for recovery programs. School is the place most kids get restoration after a cerebrum harm.

“Kay T, Lezak M. (1990). The Nature of Head Injury. In D.W. Cothell , ed. Traumatic Brain Injury and Vocational Rehabilitation. (21-65). Monomonie, WI The Research and Training Center, University of Wisconsin-Stout,

Wedel Sellars, C. and Hill Vegter, C. (2008). The Young Child: Myths and Facts about Brain Injury. (2nd Ed.). Lash Associates.”

Adapted from:

Kay T Lezak M. (1990). The Nature of Head Injury. In D.W. Cothell , ed.Traumatic Brain Injury and Vocational Rehabilitation.(21-65). Monomonie, WI: The Research and Training Center, University of Wisconsin-Stout.

Wedel Sellars, C. and Hill Vegter, C. (2008).The Young Child: Myths and Facts about Brain Injury.(2nd Ed.). Lash Associates